In a pair of studies, researchers have identified two potential therapeutic targets for hepatitis C virus. Both are related to host cells, which means they might raise fewer viral resistance issues, although experience with similar targets indicates neither is likely to be perfect.

Researchers from the University of Texas Southwestern Medical Center reported in the Proceedings of the National Academy of Sciences that assembly and secretion of very low-density lipoprotein (VLDL) is required for the secretion of HCV by host cells, while researchers from The Center for the Study of Hepatitis C at The Rockefeller University and colleagues reported in Nature that the presence of claudin-1 on liver and certain epithelial cells is necessary for HCV entry.

The way out

Although it has been known that HCV and VLDLs circulate together, a role for VLDLs in viral assembly or secretion had never been demonstrated. It also hasn't been clear why HCV production is restricted to the liver. The UT research may answer both questions.